Mitochondria are central intracellular organelles for cardiomyocytes involved in metabolism and ATP production. Heart failure is commonly accompanied by mitochondrial dysfunction. Dysfunctional mitochondria are the major source of reactive oxygen species and triggers both apoptosis and necrosis of cardiomyocytes. Since mitochondrial damage rapidly spreads through depolarization of mitochondrial membrane potential and deteriorates the function of healthy mitochondria, cardiomyocytes possess robust quality control mechanisms, and autophagy, a major mechanism of degradation of protein and organelle through lysosome, is a major mechanism to eliminate dysfunctional mitochondria. In this study, we show that general autophagy and a mitochondria-specific form autophagy (mitochondrial autophagy) are both downregulated after pressure overload and mitochondrial dysfunction develop only after mitochondrial autophagy is downregulated. Mitochondrial autophagy was induced in response to pressure overload through a mechanism dependent upon Drp1, a protein known to mediate mitochondrial fission. Treatment of the animals with TAT-Beclin 1, a peptide known to stimulate autophagy through mobilization of endogenous Beclin 1, a protein essential for autophagy, increased the level of mitochondrial autophagy in the heart and partially rescued the development of heart failure during pressure overload. These results suggest that interventions to restore the level of mitochondrial autophagy may be considered as potential treatment for heart failure patients.